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Biomedical subjects

F Stam

Publications and source records attributed to F Stam.

9 recordsLinked to original sources
PubMed2001

Effect of fluvastatin on endothelium-dependent brachial artery vasodilation in patients after renal transplantation.

BACKGROUND: Hypercholesterolemia may affect both endothelial function and arterial distensibility (DC). Renal transplant recipients (NTX) exhibit advanced structural and functional alterations of arterial vessel walls. The aim of this double-blind, randomized trial was to evaluate the effects of fluvastatin (FLU) on brachial artery flow-mediated vasodilation (FMD) and DC in hypercholesterolemic NTX. METHODS: Eighteen NTX received FLU 40 mg/day and 18 NTX placebo (PLA). Before and after six months of treatment, the brachial artery diameter and DC at rest were measured by a Doppler frequency analysis in the M mode, and then changes in diameter during reactive hyperemia (to assess endothelial-dependent FMD) and after 400 microg sublingual nitroglycerin (to assess endothelium-independent vasodilation-NMD). RESULTS: FLU, but not PLA, treatment resulted in significant decreases in total (from 288 +/- 10 to 239 +/- 8 mg/dL, P < 0.05) and low-density lipoprotein cholesterol (from 182 +/- 779 to 138 +/- 8 mg/dL, P < 0.05). Blood pressure did not differ between FLU- and PLA-treated patients and was not affected by either treatment. Also, the brachial artery baseline diameter was not different between groups and was not affected by FLU or PLA. Brachial artery flow at rest and during reactive hyperemia as measured by pulsed Doppler did not differ between groups. Brachial artery FMD increased with FLU from 0.23 +/- 0.08 to 0.54 +/- 0.08 mm (P < 0.05), whereas PLA did not alter FMD (0.22 +/- 0.07 vs. 0.14 +/- 0.05 mm at baseline and after six months of PLA treatment, respectively, P = NS). In contrast, NMD did not change significantly with either treatment (0.76 +/- 0.13 vs. 0.83 +/- 0.15 mm at baseline and after 6 months of FLU treatment, respectively, P = NS, and 0.64 +/- 0.09 vs. 0.66 +/- 0.10 mm at baseline and after 6 months of PLA treatment, respectively, P = NS). Also, brachial artery DC was not altered by FLU (6.4 +/- 1.0 vs. 5.8 +/- 0.6 x 10-3/kPa, P = NS) or PLA treatment (5.8 +/- 0.6 vs. 6.8 +/- 0.8 x 10-3/kPa, P = NS). CONCLUSIONS: In hypercholesterolemic NTX, the HMG-CoA reductase inhibitor FLU significantly improves brachial artery FMD as a measure of endothelial function after six months of treatment. In contrast, FLU does not have a beneficial effect on brachial artery DC.

Brachial Artery↗
PubMed2001

Homocysteine metabolism in renal failure.

Of the many amino acid abnormalities that are present in chronic renal failure, hyperhomocysteinemia has drawn increasing attention because of its proposed role in the development and/or progression of atherothrombotic disease. Renal function is a major determinant of fasting plasma homocysteine level, and the inverse relationship between the glomerular filtration rate (GFR) and plasma homocysteine level is present throughout the whole range of renal function. Although this suggests an active renal homocysteine metabolism, no important urinary excretion or active homocysteine extraction has been demonstrated in the human kidney. Analysis of plasma concentrations of the various cofactors and substrates of homocysteine metabolism, and the effects of different therapies indicate that an abnormal folate metabolism may be the cause of hyperhomocysteinemia in uremia. This is further supported by the finding that homocysteine remethylation, as assessed by stable isotope techniques, is impaired in dialysis patients. It is unclear whether decreased remethylation is also responsible for other abnormalities of homocysteine metabolism in renal failure such as the exaggerated rise and the impaired decline of plasma homocysteine concentration after methionine or homocysteine loading. More studies are necessary to pinpoint the precise mechanisms that lead to hyperhomocysteinemia in renal failure. This should lead to optimal treatment and, ultimately, to the prevention of cardiovascular complications in this vulnerable patient group.

5,10-Methylenetetrahydrofolate Reductase (FADH2)↗
PubMed1992

[Henoch-Schönlein purpura following treatment with streptokinase].

This article presents the clinical history of a man aged 64 who developed Henoch-Schönlein purpura after administration of streptokinase for acute myocardial infarction. Because of the increasing use of streptokinase it is assumed that type III hypersensitivity reactions to streptokinase will be seen more frequently. The first symptoms may arise after discharge from the hospital, as symptom-free periods of 3 to 21 days have been reported.

Humans↗